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Biochemical and Biophysical Research Communications, ISSN 0006-291X, 01/2019, Volume 508, Issue 3, pp. 775 - 779
Dysregulation of autophagy has been observed in obesity and type 2 diabetes. Salt-inducible kinase 2 (SIK2), a member of the AMPK-related kinase family, is... 
TFEB | Adipocytes | Autophagy | Salt-inducible kinase 2 | Autophagic flux | BIOCHEMISTRY & MOLECULAR BIOLOGY | MTOR | INDIVIDUALS | BIOPHYSICS | SIK2 | GLUCOSE-UPTAKE | OBESE | EXPRESSION | ADIPOSE-TISSUE
Journal Article
by Taub, M
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, ISSN 1422-0067, 07/2019, Volume 20, Issue 13, p. 3219
Journal Article
Molecular Cell, ISSN 1097-2765, 03/2018, Volume 69, Issue 6, pp. 1017 - 1027.e6
Journal Article
Biochemical Journal, ISSN 0264-6021, 01/2015, Volume 465, Issue 2, pp. 271 - 279
Macrophages switch to an anti-inflammatory, 'regulatory'-like phenotype characterized by the production of high levels of interleukin (IL)-10 and low levels of... 
Chemical biology | Dasatinib | Inflammation | Interleukin-10 | Salt-inducible kinase | Bosutinib | REGULATORY MACROPHAGES | PHOSPHORYLATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | IL-10 PRODUCTION | interleukin-10 | MYELOID-LEUKEMIA PATIENT | SIGNAL-TRANSDUCTION | BRUTONS TYROSINE KINASE | dasatinib | chemical biology | inflammation | salt-inducible kinase | ENDOTOXIN TOLERANCE | IN-VIVO | SELECTIVITY | bosutinib | Aniline Compounds - pharmacology | Tumor Necrosis Factor Ligand Superfamily Member 14 - immunology | Immunity, Innate - drug effects | Nitriles - pharmacology | Phosphotransferases (Alcohol Group Acceptor) - immunology | Cells, Cultured | Macrophages - cytology | Pyrimidines - pharmacology | Quinolines - pharmacology | Arginase - immunology | Animals | Protein-Serine-Threonine Kinases - antagonists & inhibitors | Cyclic AMP Response Element-Binding Protein - immunology | Protein-Serine-Threonine Kinases - immunology | Mice | Protein Kinase Inhibitors - pharmacology | Thiazoles - pharmacology | Transcription Factors - immunology | Macrophages - immunology | Cytokines - immunology | IRF, interferon regulatory factor | TLR, Toll-like receptor | IKK, IκB kinase | PGE2, prostaglandin E2 | Btk, Bruton’s tyrosine kinase | JNK, c-Jun N-terminal kinase | SIK, salt-inducible kinases | CREB, cAMP-response-element-binding protein | qPCR, quantitative real-time PCR | MSK, mitogen- and stress-activated protein kinases | HDAC, histone deacetylase | IκB, inhibitor of NF-κB | GAPDH, glyceraldehyde-3-phosphate dehydrogenase | CRTC, CREB-regulated transcription co-activator | NF-κB, nuclear factor κB | Pam3CSK4, tripalmitoylcysteinylseryl-(lysyl)4 | M-CSF, macrophage colony-stimulating factor | HA, haemagglutinin | 2, extracellular-signal-regulated kinase 1 | DMEM, Dulbecco’s modified Eagle’s medium | IL, interleukin | LPS, lipopolysaccharide | ERK 1 | TBK1, TANK-binding kinase 1 | MAPK, mitogen-activated protein kinase
Journal Article
Hypertension Research, ISSN 0916-9636, 2019, Volume 42, Issue 8, pp. 1114 - 1124
Loss of salt-inducible kinase 1 (SIK1) triggers an increase in blood pressure (BP) upon a chronic high-salt intake in mice. Here, we further addressed the... 
Hypertension | SIK1 | Sympathetic nervous system | High-salt intake | Dopamine β-hydroxylase | NETWORK | PHYSIOLOGY | BLOOD-PRESSURE | CENTRAL SODIUM | ETAMICASTAT | Dopamine beta-hydroxylase | TRANSPORT | PERIPHERAL VASCULAR DISEASE | DOPAMINE-RECEPTORS | KIDNEY | EXPRESSION
Journal Article
Journal Article
EMBO reports, ISSN 1469-221X, 07/2017, Volume 18, Issue 7, pp. 1166 - 1185
A pathologic osteochondrogenic differentiation of vascular smooth muscle cells ( VSMC s) promotes arterial calcifications, a process associated with... 
histone deacetylase | smooth muscle cell | vascular calcification | HDAC4 | CELLS | CONTROLS CHONDROCYTE HYPERTROPHY | ACETYLATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | DEFICIENCY | CELL BIOLOGY | ARTERIAL CALCIFICATION | DISEASE | OSTEOBLASTS | EXTRACELLULAR-MATRIX | EXPRESSION | Up-Regulation | Cytoskeletal Proteins - genetics | Protein-Tyrosine Kinases - metabolism | Humans | Vascular Calcification - genetics | Cytoplasm - metabolism | Protein-Tyrosine Kinases - genetics | Vascular Calcification - physiopathology | Cell Differentiation | Intracellular Signaling Peptides and Proteins - genetics | Protein-Serine-Threonine Kinases - metabolism | Repressor Proteins - metabolism | Cytoplasm - chemistry | Histone Deacetylases - genetics | Signal Transduction | Gene Expression Regulation | Protein-Serine-Threonine Kinases - genetics | Aortic Valve - physiopathology | Repressor Proteins - genetics | Histone Deacetylases - metabolism | Muscle, Smooth, Vascular - pathology | Animals | Adaptor Proteins, Signal Transducing - genetics | LIM Domain Proteins - genetics | Mice | Cell Nucleus | Calcification (ectopic) | Histone deacetylase | Salts | Smooth muscle | Valves | Pharmacology | Nuclei | Morbidity | Pathology | Biomedical materials | Salt-inducible kinase | Rodents | Calcification | Aorta | Cytoskeleton | Biocompatibility | Inhibition | Position (location) | Localization | Differentiation | Cytoplasm | Chromatin, Epigenetics, Genomics & Functional Genomics | Post-translational Modifications, Proteolysis & Proteomics | Molecular Biology of Disease
Journal Article
The FEBS Journal, ISSN 1742-464X, 02/2018, Volume 285, Issue 3, pp. 467 - 480
The salt‐inducible kinase ( SIK ) family regulates cellular gene expression via the phosphorylation of cAMP‐regulated transcriptional coactivators ( CRTC s)... 
14‐3‐3 protein | protein phosphorylation | catalytic activity | transcriptional regulation | 14-3-3 protein | LOCALIZATION | CREB | STRUCTURAL BASIS | PHOSPHORYLATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | TRANSCRIPTION | LKB1 | Protein Kinases - metabolism | Phosphorylation | Protein Kinases - genetics | Transcription Factors - chemistry | Humans | Protein Kinases - chemistry | Substrate Specificity | Recombinant Fusion Proteins - metabolism | HEK293 Cells | Protein-Serine-Threonine Kinases - antagonists & inhibitors | Conserved Sequence | Protein Interaction Domains and Motifs | Active Transport, Cell Nucleus | Binding Sites | Cyclic AMP - metabolism | Peptide Fragments - genetics | Protein-Serine-Threonine Kinases - metabolism | Cyclic AMP-Dependent Protein Kinases - metabolism | Peptide Fragments - metabolism | Protein-Serine-Threonine Kinases - genetics | Recombinant Fusion Proteins - chemistry | Transcription Factors - genetics | 14-3-3 Proteins - metabolism | Transcription Factors - metabolism | Peptide Fragments - chemistry | Animals | Peptide Fragments - antagonists & inhibitors | Mice | Protein Processing, Post-Translational | Protein-Serine-Threonine Kinases - chemistry | Mutation | Transcription Factors - agonists | Amino Acid Substitution | Proteins | Cyclic adenylic acid | Protein binding | Protein kinase A | Repressing | Salts | Transcription | Cyclic AMP | Substrate inhibition | Catalytic activity | Kinases | Gene expression | Substrates | Signaling | Evolutionary conservation | Salt-inducible kinase | Catalysis | Binding sites | Cytoplasm
Journal Article
Clinical Cancer Research, ISSN 1078-0432, 04/2017, Volume 23, Issue 8, pp. 1945 - 1954
Journal Article